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Interleukin-6 as a mechanism for the adverse effects of social stress on acute Theiler's virus infection
- Source :
- Brain, behavior, and immunity. 21(8)
- Publication Year :
- 2006
-
Abstract
- Prior exposure to social disruption stress (SDR) exacerbates both the acute and chronic phase of Theiler’s murine encephalomyelitis virus infection (TMEV; [Johnson, R.R., Storts, R., Welsh, T.H., Jr., Welsh, C.J., Meagher, M.W., 2004. Social stress alters the severity of acute Theiler’s virus infection. J. Neuroimmunol. 148, 74--85; Johnson, R.R., Prentice, T.W., Bridegam, P., Young, C.R., Steelman, A.J., Welsh, T.H., Welsh, C.J.R., Meagher, M.W., 2006. Social stress alters the severity and onset of the chronic phase of Theiler’s virus infection. J. Neuroimmunol. 175, 39--51]). However, the neuroimmune mechanism(s) mediating this effect have not been determined. The present study examined whether stress-induced increases in the proinflammatory cytokine interleukin-6 (IL-6) contributes to the adverse effects of SDR on acute TMEV infection. Experiment 1 demonstrated that SDR increases central and peripheral levels of IL-6 and that this effect is reversed by intracerebral ventricular infusion of neutralizing antibody to IL-6 prior to each of six SDR sessions. Although SDR reduced the sensitivity of spleen cells to the anti-inflammatory effects of corticosterone, the neutralizing antibody to IL-6 did not alter this effect. To investigate whether stress-induced increases in IL-6 contribute to the exacerbation of acute TMEV infection, Experiment 2 examined whether intracerebral administration of neutralizing antibody to IL-6 during SDR would prevent the subsequent exacerbation of acute TMEV infection. Experiment 3 then replaced the social stress with intracerebral infusion of IL-6 to assess sufficiency. As expected, prior exposure to SDR subsequently increased infection-related sickness behaviors, motor impairment, CNS viral titers, and CNS inflammation. These deleterious effects of SDR were either prevented or significantly attenuated by intracerebral infusion of neutralizing antibody to IL-6 during the stress exposure period. However, infusion of IL-6 alone did not mimic the adverse effects of SDR. We conclude that IL-6 is necessary but not sufficient to exacerbate acute TMEV infection.
- Subjects :
- Male
Multiple Sclerosis
Exacerbation
Neuroimmunomodulation
Immunology
Motor Activity
Social Environment
Virus
Article
Proinflammatory cytokine
Behavioral Neuroscience
chemistry.chemical_compound
Mice
Corticosterone
Theilovirus
Cardiovirus Infections
Medicine
Animals
Neutralizing antibody
Interleukin 6
Glucocorticoids
Social stress
Analysis of Variance
Mice, Inbred BALB C
biology
Endocrine and Autonomic Systems
business.industry
Interleukin-6
Multiple sclerosis
Sick Role
Brain
medicine.disease
Disease Models, Animal
chemistry
Spinal Cord
biology.protein
Exploratory Behavior
business
Spleen
Stress, Psychological
Subjects
Details
- ISSN :
- 08891591
- Volume :
- 21
- Issue :
- 8
- Database :
- OpenAIRE
- Journal :
- Brain, behavior, and immunity
- Accession number :
- edsair.doi.dedup.....d9db92d7575a95e2762e977f9d7ef398